Cardiac arrhythmias

Contributed by Dr Rajiv Sankaranarayanan, a cardiology specialty registrar in electrophysiology, Manchester Heart Centre, Manchester.

Junctional bradycardia: ECG shows absence of P waves and heart rate of 40bpm
Junctional bradycardia: ECG shows absence of P waves and heart rate of 40bpm

Section 1: Epidemiology and aetiology
Cardiac arrhythmias affect more than two million people in the UK, leading to approximately 100,000 sudden cardiac deaths each year.1

Cardiac arrhythmia is defined as any inherited or acquired abnormality of normal heart rate or rhythm. The normal heart rate is defined as 60-100bpm at rest, decreasing during sleep by an average of 24bpm in young adults and by 14bpm in those over 80 years of age.

Normal sinus rhythm is defined as a normal heartbeat initiated by a normal cardiac pacemaker within the sino-atrial node and presenting on ECG as a regular rhythm with a rate within the normal range, normal P wave before each QRS complex, normal PR interval and normal QRS duration.

Bradyarrhythmia can be sub-classified into two groups: sinus node disease and artrioventricular (AV) conduction abnormalities.

Sinus node disease encompasses sinus bradycardia (regular rhythm with normal P waves on ECG preceding each QRS complex and a sinus node depolarisation rate of <60 bpm), sinus arrest (failure of impulse formation), sino-atrial exit block (failure of exit of impulse from sinus node to atrial tissue), and tachycardia-bradycardia syndrome leading to slow atrial and ventricular rates alternating with atrial tachyarrhythmias.

AV conduction abnormalities involve varying degrees of block in the AV node (AVN), bundle of His, right or left bundle branches and anterior or posterior fascicles of the left bundle branch.

AV block is sub-classified as first, second or third degree.

The above can also exist in combination.

Tachyarrhythmias are caused by re-entry, abnormal automaticity or triggered activity. They can be sub-classified into supraventricular or ventricular.

Supraventricular tachyarrhythmia (SVT) originates within atrial or AVN tissue.

AF is the most common sustained cardiac arrhythmia with >46,000 cases/year diagnosed in the UK.2 It is characterised by multiple re-entrant wavelets in the atria. The prevalence rises with age from 1.5 per cent in 60-year-olds to more than 10 per cent in those over 90 years.3

The prevalence of paroxysmal SVT excluding AF, atrial flutter and atrial tachycardia (AT) is 2.25 cases per 1,000 persons, with an incidence of 35 per 100,000 person-years.4

AV node re-entrant tachycardia (AVNRT) is caused by persistence of dual AVN physiology (two AVN pathways with differential electrophysiological properties). The onset is triggered by an atrial premature beat (APB).

AV re-entry tachycardia (AVRT), such as Wolff Parkinson White (WPW) syndrome, is caused by the presence of an accessory atrioventricular pathway that bypasses the AVN. The prevalence on ECG is 0.1-3 per 1,000 tracings.5

Ventricular tachyarrhythmias
Ventricular premature beats (VPBs) are the most common ventricular arrhythmias. They are ectopic impulses arising distal to the His-Purkinje system. Ventricular tachycardia (VT) is defined as a broad complex tachyarrhythmia with at least three VPBs at a heart rate of 120bpm (non-sustained if lasting <30 seconds; sustained if requires cardioversion or lasts >30 seconds).

Common causes of arrhythmia
  • Bradyarrhythmia
  • Tachyarrhythmia
  • Increased vagal tone/reactivity
  • IHD, acute MI
  • Ageing (defenerative)
  • Aortic stenosis. Mitral valve prolapse
  • Cardiomyopathy and IHD
  • Cardiomyopathy
  • Metabolic conditions - hypothyroidism
  • Congenital heart disease
  • Congenital heart blocks
  • Electrolyte disturbance
  • Myotonic dystrophy
  • Long QT syndrome

Section 2: Diagnosis
The presence or absence of symptoms in bradyarrhythmias depends on the cardiac output (stroke volume x heart rate).

Increase in stroke volume may compensate for low heart rates and thereby prevent onset of symptoms with even complete heart block.

There can be non-specific symptoms, such as lethargy, muscle weakness, confusional states due to cerebral hypoperfusion or more typical symptoms, such as pre-syncope or syncope.

Underlying conditions
A history of possible precipitant factors, symptoms of underlying ischaemia, heart failure, a history of exertional syncope or family history of sudden death, should be elicited.

Whether tachyarrhythmias lead to symptoms, depends on underlying structural heart disease and the haemodynamic reserve. Patients with adequate reserve may be entirely asymptomatic.

APBs and VPBs are usually asymptomatic or may be felt as missed beats or palpitations. AVNRT, AVRT and VT are recurrent with typically abrupt onset and offset.

Pre-syncope or syncope (in 15 per cent of SVT) is commonly seen in elderly patients with tachybrady syndrome (due to a long pause after abrupt termination of the tachycardia), SVT with very fast ventricular rates, VT, structural heart disease, such as hypertrophic cardiomyopathy or severe aortic stenosis, or due to AF with rapid conduction over accessory AV pathways, which particularly can degenerate into VF and lead to sudden death. SVTs can also exacerbate underlying ischaemia or heart failure (tachycardiomyopathy).

General physical examination during bradyor tachyarrhythmia may reveal signs of haemodynamic instability, such as hypotension or signs of congestive cardiac failure as well as the likely precipitating causes.

Patients with AF or premature beats have an irregularly irregular pulse. ECG during arrhythmia is crucial in making the diagnosis.

Analysis of RP interval can help to classify SVTs as short RP and long RP tachycardia. Short RP SVTs have the P wave either obscured by QRS or occurring in the last part of QRS or ST segment such that RP interval is less than half the RR interval. Long RP SVTs have the P wave located just before the next QRS complex such that RP interval is more than half the RR interval. Attempt to distinguish between VT and SVT. If there is any doubt, treat as VT.

Electrolytes, TFTs, inflammatory markers, coagulation profile prior to initiating warfarin, and troponin (if ischaemic precipitant suspected) are required. ECG during arrhythmia is crucial.

If the arrhythmia has not been captured on 12-lead ECG, 24-hour Holter, one week Holter monitoring or one month event monitoring is used to correlate symptoms with possible arrhythmias, depending on frequency of symptoms.

If symptoms are rare, implantable loop recorders can be used. Carotid sinus massage has a role to assess autonomic function in bradyarrhythmia.

Exercise testing can assess chronotropic response in bradyarrhythmias and tachyarrhythmias if an exertional or ischaemic precipitant is suggestive.

Electrophysiological testing is also useful in diagnosing and risk-stratifying arrhythmias.

Section 3: Management
Novel ECG techniques are useful in stratifying patients at risk of sudden cardiac death due to ventricular arrhythmias. These include microvolt T wave alternans (beat to beat fluctuation in T wave morphology and amplitude); signal averaged ECG (computerised averaging of ECG complexes to facilitate the detection of small microvolt signals called ventricular late potentials) and heart rate variability (physiological phenomenon of variation in time interval between heart beats) or turbulence (response of the sinus node to VPBs).

Identifying a potentially reversible cause of bradyarrhythmia is very important as this may avoid the need for temporary or permanent pacing.

Patients presenting with symptomatic prolonged pauses (more than 3 seconds) on Holter monitoring, Mobitz 2 AV block (due to risk of degeneration into complete heart block) or complete heart block, require urgent hospital admission.

However, stable patients with other symptomatic bradyarrhythmias can be referred electively.

Treatment of tachyarrhythmias
Premature beats can be prevented by avoidance of precipitating factors like nicotine, alcohol, lack of sleep, caffeine, stress or treatment of other general conditions.

Adenosine usually terminates 90 per cent of AVNRT. If this fails, IV verapamil or beta-blocker can be given.

Patients with troublesome AVNRT recurrences despite antiarrhythmics or patients intolerant to medications are offered slow pathway ablation (>90 per cent cure rate).

In AVRT, such as WPW syndrome, AVN blocking agents such as adenosine, digoxin, verapamil and diltiazem can increase conduction along the accessory pathway during AF, precipitating VF and therefore are contraindicated.

WPW patients with SVT can be treated with IV flecainide or IV procainamide or DC cardioversion can be used instead. WPW presenting with AF should be treated with urgent DC cardioversion.

Catheter ablation is the treatment of choice to prevent the recurrence of tachycardias but amiodarone or sotalol could be used in the interim.

Pulmonary vein isolation by catheter ablation can be considered to treat AF in drug-intolerant patients or for drug-refractory symptoms. It has a higher success rate in young patients with lone paroxysmal AF.

AV node ablation and pacemaker implant (ablate and pace) can be considered generally in elderly patients with treatment-resistant symptomatic permanent AF.

Catheter ablation is also the treatment of choice for recurrent, symptomatic paroxysmal or permanent AT, typical atrial flutter or symptomatic WPW.

Treatment of ventricular arrhythmias
If the patient is haemodynamically stable, electrical cardioversion is preferred as IV amiodarone is unpredictable in its efficacy or onset of action.

Beta-blockers, ACE inhibitors, angiotensin receptor blockers and spironolactone have all been shown to reduce the incidence of sudden cardiac death due to ventricular arrhythmias.

Torsades is treated by withholding any QT prolonging precipitant, administering IV magnesium or overdrive pacing. VF is treated with emergency defibrillation and CPR as per ALS guidelines.

Section 4: Developments in therapy
Dronedarone is currently a part of draft NICE guidance for treatment of non-permanent AF. New antiarrhythmics under development include celivarone (another amiodarone analogue) and vernalakant (atrial-selective antiarrhythmic for cardioversion of AF).

Potential alternatives to warfarin include the oral direct thrombin inhibitor dabigatran (advantages include fixed dosing, lack of need for routine monitoring and possible increased efficacy) and the anti-Xa drug rivaroxaban. Also, a plug in the left atrial appendage may be used to prevent clot formation (Watchman device).

Catheter ablation has come into prominence in treatment of symptomatic VT in structurally normal hearts, scar-related incessant VT leading to frequent shocks or 'VT storms' as well as to treat idiopathic VF.

MRI-compatible pacemakers and defibrillators are under development. Ongoing research in the interventional electrophysiology field includes new energy sources, such as laser, ultrasound and cryothermy, balloon-based catheters and magnetic navigation systems for complete remote controlled 3D mapping, imaging and ablation.

Follow up
A patient with recurrent syncope or documented VT may require urgent assessment or referral to a heart rhythm specialist.

1. National Service Framework Chapter 8 - Arrhythmias and sudden cardiac death - implementation (published 4 March 2005).

2. Ruigomez A et al. Incidence of chronic atrial fibrillation in general practice and its treatment pattern. J Clin Epidemiol 2002; 55: 358-63.

3. van Weert HC. Diagnosing atrial fibrillation in general practice. BMJ 2007; 335(7616): 355-6.

4. Orejarena LA, Vidaillet H Jr, DeStefano F et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol 1998; 31(1): 150-7.

Further Resources
ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). European Heart Rhythm Association; Heart Rhythm Society, Zipes DP, Camm AJ, Borggrefe M et al. J Am Coll Cardiol. 2006; 48(5): e247-346.

ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation-executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation). Fuster V, Ryden LE, Cannom DS et al. Eur Heart J. 2006; 27(16): 1979-2030.

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